The document discusses various types of shock, including hypovolemic, cardiogenic, septic, anaphylactic, and neurogenic shock, detailing their causes, pathophysiology, and clinical presentations. It emphasizes critical mechanisms necessary for maintaining circulatory homeostasis and the progression from initial compensatory phases to irreversible stages of shock. Management strategies are outlined, highlighting the importance of timely intervention and the varying prognoses based on the type and duration of shock.

1. Arpita Halder.
Associate professor.
College and School of Nursing R.N.Tagore
Hospital.

2.  Shock results from the failure of the cardiovascular
system to provide sufficient blood circulation.
 To maintain circulatory homeostasis the following
mechanisms must be present –
 1. a functioning of heart to circulate blood .
 A sufficient amount of blood volume .
 The capability of the vascular system , accommodating
blood flow to the capillaries and returning to the right
side of the heart.

3. DEFINATION
Shock give rise to systemic hypoperfusion caused by reduction either in
cardiac output or in effective circulatory blood volume.
End results are :
Hypotension
Tissue hypoperfusion
Cellular hypoxia
Reversible injury
Irreversible injury with persistent of shock
End organ dysfunction
Death

4. Shock
Cardiogenic shock.
Hypovolemic shock.
Distributive shock( neurogenic , anaphylactic, septic)
Obstructive shock
Systemic inflammatory response syndrome(SIRS)
Mediator excess: cytokines ( tumor necrosis factor ,
interleukins, oxygen free radicals .)
Wide spread endothelial injury and dysfunction .
Vasodilation and increased capillary permeability .
Tissue edema .
Neutrophil entrapment in microcirculation .

5. Multi organ dysfunction syndrome (MODS)
Target organs
Cardiovascular dysfunction .
Lung dysfunction .
GI dysfunction.
Liver dysfunction .
CNS dysfunction .
Renal dysfunction .
Skin dysfunction .

6. TYPES OF SHOCK
 Hypovolumic shock
 Cardiogenic shock
 Septic shock
 Anaphylactic shock
 Neurogenic shock

7. HYPOVOLUMIC SHOCK
Hypovolumic shock occurs due to rapid reduction in blood
volume or plasma volume.
Causes of hypovlumic shock :
1. Hemorrhage
2. Severe dehydration-severe vomiting, severe diarrhea
3. Severe burn
4. Abdominal ascities
5. Acute pancreatitis
6. Diabetes mellitus
7. Over use of Diuretics

8. HYPOVOLUMIC SHOCK
 Pathophysiology of hypovolumic shock :
Dehydration, Hemorrhage
Reduction in intravascular blood volume
Decreased pre-load
Decreased stroke volume & CO
Systemic hypoperfusion
Compensatory vasoconstriction
Tissue ischemia, hypoxia
Cellular & organ dysfunction

9. Cont..
 Hypovolemic shock can be two types – Absolute
hypovolemic – external loss of whole blood .( trauma,
surgery). Or loss of other body fluids ( vomiting
,diarrhea).
 Relative hypovolemic – pooling of blood or fluids.(
bowel obstruction)
 Fluid shift .( burn)
 Internal bleeding .( fracture.)
 Massive vasodilation ( sepsis.)

10. Hypovolemic shock
 Cardiovascular change- Preload
Stroke volume.
Capillary refill .
Pulmonary system- bradypnea.
Renal system- decreased urine output.
Skin- pallor ,cool, clammy .
Neurologic system- decreased perfusion.
GI system- absent bowel sounds.

11. Diagnostic finding
 Hematocrit.
 Hemoglobin.
 Lactate.
 Urine specific gravity.
 Changes in electrolyte.

12. CARDIOGENIC SHOCK
 Cardiogenic shock is characterized by reduced pumping
ability of heart due to intrinsic myocardial damage or
extrinsic or obstruction to out flow. It is most commonly
occurs in association with and as a direct result of acute
myocardial ischemia.
 Incidence:
-Cardiogenic shock occurs in 8.6% of patient with ST
segment elevation.
-Myocardial ischemia with 29% of those presenting to the
hospital already in shock.
-2% of non ST segment elevation MI.

13. CARDIOGENIC SHOCK
 Risk factor :
-Pre existing myocardial damage
-Diabetes Mellitus
-Advanced age
-Previous MI
-Dysarythmia

14. CARDIOGENIC SHOCK
Causes of Cardiogenic shock :
 MI
 Vulvular regurgitation
 Acute myocarditis
 Cardiomyopathy
 Cardiac tamponade
 Pulmonary embolism
 Acute vulvular dysfunction
 Cardiac dysarythmia
 Rupture ventricular aneurysm
 Beta-blocker overdose
 Ca-channel blocker overdose

15. CARDIOGENIC SHOCK
Pathophysiology of cardiogenic shock :
Myocardial Infraction
Myocardial ischemia or injury Myocardial dysfunction
Systemic inflammatory response Decreased CO & stroke volume
Increased NO synthesis Systemic hypoperfusion Hypotension
Vasodilatation Decreased coronary perfusion
Compensatory vasoconstriction Cardiac & other end organ damage
Progressive myocardial dysfunction
Death

16.  Cardiac marker increased.
 B-type natriuretic peptide.
 Blood glucose .
 BUN.
 ECG.
 Chest x-ray .

17. SEPTIC SHOCK
 Sepsis is a clinical state that accompanies infection either
confined to a local site from which toxin are absored or
associated with invasion of organism in to the blood
stream.
 Causes of septic shock:
-Overhelming microbial infection
-Gram +ve septicemia
-Endotoxic shock (Gram –ve septicemia)
-Fungal sepsis
-Super antigen

18. SEPTIC SHOCK
 Predisposing factor :
 Increased life support for high risk patient
 Advanced age
 Debilitating illness
 Increasing use of invasive procedure
 Disseminated malignancy
 Increased number of immuno-compromised host
-Secondary to malignancy
-Immuno-supression
-HIV infection

19. SEPTIC SHOCK
Microbiology :
Gm +
Staphylococcus
Streptococcus
Gm -
E.Coli
Klebsiella
Proteus
Other
Fungi

20. SEPTIC SHOCK
Pathophysiology of septic shock :
Bacterial infection
Endotxin ( LPS ) & other microbial products
Binds to LPS binding protein in serum
Binds to CD14 receptors on mononeuclear cells
CD14 binds to TLR4
Release of chemical mediators

21. SEPTIC SHOCK
Pathophysiology of septic shock :

22. SEPTIC SHOCK
 Patho-physiology of septic shock :
In septic shock systemic vasodilatation and pooling of
blood in the periphery leads to tissue hypo perfusion
and though the cardiac out put is preserved this is
accompanying widespread endothelial cell activation
and often leads to hablypercoagulable state that can
manifest DIC.Septic shock is associated with change
in metabolism that can directly suppress cellular
function. The net effect is hypo perfusion and
dysfunction of multi-organ.

23. SEPTIC SHOCK
 Major factors contributing to the pathophysiology of septic shock are
following.
 Inflammatory mediators;
Various microbial cell wall contains lipopolysaccaride are
released when the cell wall are degraded. Free LPS bind to circulatory
LPS.This complex then binds to a cell surface receptor CD14 on
macrophage, mononuclear paghocytic cell, endothelial cell.CD14 binds
to the signal transducing protein TLR-4.Upon activation cascade of
cytokines mediators TNF,TL-1,IL-8,INF- .The compliment cascade are
activated directly or through proteolytic activity of plasmin resulting in
production of anaphylotoxins C3a&C5a,chemotatctic factor C5a causes
vasodilatation & increases vascular permeability.Activated endothelial
cell and macrophage release NO contribute to pro-inflammatory state.

24. SEPTIC SHOCK
 Endothelial cell activation and injury:
Endothelial cell activation by microbial products or
inflammatory mediators produced by leukocytes. Has 3
major sequele-thrombosis,increase vascular
permiability,vasodilation
Pro-inflammatory cytokines result in increased tissue
factor production by endothelial cell and monocyte.The
production of endothelial anti-coagulant factor-tissue
factor pathway inhibator,thrombomodulin and protein-C
reduced.Reduced blood flow at the level of small vessels'
produce stasis that reduce the wash out of activated
coagulation factor results in deposition of fibrin rich
thrombi in small vessels, that lead to tissue hypoperfusion..

25.  In DIC increase consumption of coagulation factor &
platelet leads to bleeding & hage.
 Increase vascular permiability leads exudation of fluid
in to interstitum causing oedema.
 Endothelium increase the relase of NO.

26. SEPTIC SHOCK
 Metabolic abnormalities:Septis patient exhibit insulin
resistance and hypoglycemia. Cytokines such as TNF &
IL-1,stress induced
hormone(glucagon,catecholamines)all drive
gluconeogenesis.At the same time the pro-
inflammatory cytokines suppress insulin release while
simultaneously promoting insulin resistance in the
liver & other tissue, by surface expression of glucose
transporter. Hyperglycemia reduced neutrophil
function & bactericidal activity. Sepsis also related
with adrenal insufficiency & factional deficency of
glucocortcoid.

27. SEPTIC SHOCK
 Immuno suppression:
hyper inflammatory state activate immuno-
suprssion mechanism which involve both innate &
adaptive immunity by production of anti-
inflammatory mediators(soluable TNF receptors,IL-
recepor antagonist& IL-10).
Organ dysfunction:
Systemic hypotension, interstitial edema, small
vessels thrombosis reduce the delivery of oxygen &to
the tissue.

28. SEPTIC SHOCK
 High level of cytokines, secondary mediators reduces
myocardial contractility & CO. Increase vascular
permeability & endothelial injury acute respiratory
distress syndrome ultimately cause multiple organ
failure.

29. Toxic shock syndrome:
Toxic shock syndrome is a potentially fatal illness
caused by bacterial toxin(super antigen) released by –
Staphylococcus aureus & Streptococcus pyogens.
Streptococcal TSS associated with recent soft tissue
injury like surgery,pharyngitis,NSAID drug use.
Staphylococcal TSS observe mostly among
menstruating women, but also associated with cutaneous
infection, post-partum & C/S wound infection & focal
staphylococcal infection like abscess,empyma,pneumonia.

30. NEUROGENIC SHOCK
Neurogenic shock occurs in the setting of anesthetic
accident or spinal cord injury causes loss of vascular
tone and peripheral pulling of blood.

31. Pathophysiology .
 Disruption of sympathetic nervous system.
 Loss of sympathetic tone.
 Venous and arterial vasodilation.
 Decreased BP.
 Decreased venous return.
 Decreased stroke volume .
 Decreased cardiac output.
 Decreased cellular oxygen supply.
 Decreased tissue perfusion.
 Impaired cellular metabolism.

32. ANAPHYLACTIC SHOCK
In Anaphylactic shock,decreased systemic vascular
resistance due primarily to massive histamine release
from mast cell after activation of IgE mediated
hypersensitivity reaction as well as increase synthesis
of prostaglandin. That leads to vasodilatation and
increase vascular permiability.Ultimate results are
systemic hypotension, tissue perfusion and cellular
anoxia.

33. ANAPHYLACTIC SHOCK
 Causes of anaphylactic shock:
1.Iatrogenic( drug)
2.Accidental exposure to an allergen and co-exiting
respiratory complaints(wheezing & dyspnea)& or purities.
 Systemic inflammatory response in anaphylactic shock:
Respiratory distress
Wheezing
Urticarial rash
Angioedema.

34. STAGES OF SHOCK
1.An initial non progressive phage ( compensatory
stage)
2.A progressive stage
3.An irreversible stage

35.  An initial non progressive phage:
In this phage a varieties of neuro-hormonal &
haemostatic mechanism helps to maintain cardiac
out-put & blood pressure. These includes:
- Baro-receptor reflex mechanism
- Release of catecholamine's
- Activation of Renin-angiotension axis
- Anti-diuretic hormone release
-Generalized sympathetic activation

36.  Net effects are- 1.Tachycardia
2.Peripheral vasoconstriction
3.Renal conservation of fluid
Resulting in restoration of circulation and tissue
perfusion.

37.  Progressive phase:
If the compensatory mechanism fails to restore
circulation, vital organ shows the effects of
hypoxia.Persistant oxygen deficiency leads to intra
cellular anaerobic glycolysis with lactic acidosis,thus
reduce tissue pH and vasomotor response. Resulting
reduce cardiac output and anoxic injury to endothelial
cell leads to DIC.

38.  Irreversible stage:
When there is failure to restore circulation either
by compensatory mechanism or by therapeutic
intervention,the process of shock enters the
irreversible stage. Wide spread cell injury is reflected
in lysosomal enzyme lekage,nitric oxide reduced
myocardial contractility,acute tubular necrosis
ultimately death.

39. MORPHOLOGY OF SHOCK
 Since shock is characterized by failure of multi-organ
systems, the cellular changes may appear in any tissue.
Brain: ischemic encephalopathy.
Heart: coagulative necrosis or subendocardial hemorrhage
or contraction band necrosis.
Kidney: acute tubular necrosis.
Lung: diffuse alveolar damage develop shock lung.
Gastrointestinal tract: Hemorrhagic enteropathy.
Adrenal gland: cortical cell lipid depletion may occur.
Liver: fatty change, central hemorrhagic necrosis.

40. CLINICAL PRESENTATION OF SHOCK
 Altered mental status-
Restless,confusion,stupor,coma,agitation
 Patient may unconscious or semi-conscious
 Pallor
 Increase sweating
 Cold clammy skin. Warm in septic shock
 Pulse-Tachycardia, rapid weak thready pulse
 Respiration-Tachypnia, slow and regular
 Blood pressure-low blood pressure
 Temperature may or may not be raised
 Dehydration
 Reduce urine output

41. DIAGNOSIS OF SHOCK
 History taking
 General and physical examination
 Vital sign assessment

42. LAB DIAGNOSIS
 CBC
 Biochemical test-serum electrolyte,ramdom blood
sugar,s.creatinine
 ECG
 Chest x-ray
 Blood culture, urine R/M/E & C/S,sputum for gram
stain & C/S
 Blood grouping & Cross matching
 Cardiac enzyme
 Arterial blood gas analysis

43. MANAGEMAENT OF SHOCK
 Admitted in intensive care unit
 Ensure ABC
Clear airway, adequate breathing, assessment of circulation-
pulse,BP,urine volume.
 Position of the patient
Trendelenburg or supine position to increase cerebral blood
flow.
 Oxygenation-High flow oxygen should be delivered.
 Establish IV access
 Restore circulatory blood volume-blood in case of
bleeding,crystalioid(n/s,ringer’ s lactate )
cont..

44.  Vasoactive drugs
Dopamine with or with out dobutamine provide
ionotropic support increasing perfusion of the ischemic
myocardium &all body tissue.
 Surgical intervention if needed.
 Insulin therapy in case of hyperglycemia
 Treatment of underlying cause:
Broad spectrum antibiotic coverage in case of infection.
Cardiogenic shock-treatment according to cause such as
MI or left ventricular failure.
Hypovolumic shock-adrenalin I/m Hydrocortisone

45.  In acute adrenal insufficiency-Corticosteroid use as
life saving drug.
 Activated protein-C can be use in severe sepsis.

46.  The prognosis varies with the origin of shock and its
duration.
 80%-90% of young with hypovolumic shock survive
with appropiate management.
 Cardiogenic shock associated with extensive
myocardial infraction mortality rate up to 75%
 Septic shock -mortality rate up to 75%
PROGNOSIS OF SHOCK